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Pace, E. et al.

Elisabetta Pace, Maria Ferraro, Carina Gabriela Uasuf, Antonino Giarratano, Stefania La Grutta, Giuseppe Liotta, Malcolm Johnson, Mark Gjomarkaj,

Cilomilast counteracts the effects of cigarette smoke in airway epithelial cells.

Cigarette smoke extracts (CSE) alter TLR4 expression and activation in bronchial epithelial cells. Cilomilast, a phosphodiesterase-4 inhibitor, inhibits cigarette smoke-induced neutrophilia. This study was aimed to explore whether cilomilast, in a human bronchial epithelial cell line (16-HBE), counteracted CSE effects. In particular, TLR4 expression, IP-10 and IL-8 release, lymphocyte and neutrophil chemotactic activity and ERK and IkBa phosphorylation in CSE and LPS-stimulated 16-HBE were assessed. CSE increased TLR4 expression, reduced IP-10 release and lymphocyte chemotactic activity and increased IL-8 release and neutrophil chemotactic activity. Cilomilast reduced TLR4 expression, IL-8 release and neutrophil chemotactic activity as well as it increased IP-10 release and lymphocyte chemotactic activity. All these cilomilast mediated effects were associated with a reduced ERK1/2 and with an increased IkBa phosphorylation. In conclusion, the present study provides compelling evidences that cilomilast may be considered a possible valid therapeutic option in controlling inflammatory processes present in smokers.[1]

References

Cilomilast counteracts the effects of cigarette smoke in airway epithelial cells. Pace, E., Ferraro, M., Uasuf, C.G., Giarratano, A., La Grutta, S., Liotta, G., Johnson, M., Gjomarkaj, M. Cell. Immunol. (2011) [Pubmed]

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